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• Research Paper Volume 12, Issue 24 pp 24778-24797

  L-PGDS deficiency accelerated the development of naturally occurring age-related osteoarthritis

  Relevance score: 15.127493

  Yassine Ouhaddi, Mehdi Najar, Frédéric Paré, Bertrand Lussier, Yoshihiro Urade, Mohamed Benderdour, Jean-Pierre Pelletier, Johanne Martel-Pelletier, Hassan Fahmi

  Keywords: osteoarthritis, cartilage, aging, PGD2, L-PGDS

  Published in Aging on December 23, 2020

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  Osteoarthritis (OA) is the most common musculoskeletal disorder among the elderly. It is characterized by progressive cartilage degradation, synovial inflammation, subchondral bone remodeling and pain. Lipocalin prostaglandin D synthase (L-PGDS) is responsible for the biosynthesis of PGD₂, which has been implicated in the regulation of inflammation and cartilage biology. This study aimed to evaluate the effect of L-PGDS deficiency on the development of naturally occurring age-related OA in mice.

  OA-like structural changes were assessed by histology, immunohistochemistry, and micro–computed tomography. Pain related behaviours were assessed using the von Frey and the open-field assays.

  L-PGDS deletion promoted cartilage degradation during aging, which was associated with enhanced expression of extracellular matrix degrading enzymes, matrix metalloprotease 13 (MMP-13) and a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS-5), and their breakdown products, C1,2C, VDIPEN and NITEG. Moreover, L-PGDS deletion enhanced subchondral bone changes, but had no effect on its angiogenesis. Additionally, L-PGDS deletion increased mechanical sensitivity and reduced spontaneous locomotor activity. Finally, we showed that the expression of L-PGDS was elevated in aged mice. Together, these findings indicate an important role for L-PGDS in naturally occurring age-related OA. They also suggest that L-PGDS may constitute a new efficient therapeutic target in OA.